As part of their life cycle, neutralophilic bacteria are often exposed to varying environmental stresses, among which fluctuations in pH are the most frequent. In particular, acid environments can be encountered in many situations from fermented food to the gastric compartment of the animal host. Herein, we review the current knowledge of the molecular mechanisms adopted by a range of Gram-positive and Gram-negative bacteria, mostly those affecting human health, for coping with acid stress. Because organic and inorganic acids have deleterious effects on the activity of the biological macromolecules to the point of significantly reducing growth and even threatening their viability, it is not unexpected that neutralophilic bacteria have evolved a number of different protective mechanisms, which provide them with an advantage in otherwise life-threatening conditions. The overall logic of these is to protect the cell from the deleterious effects of a harmful level of protons. Among the most favoured mechanisms are the pumping out of protons, production of ammonia and proton-consuming decarboxylation reactions, as well as modifications of the lipid content in the membrane. Several examples are provided to describe mechanisms adopted to sense the external acidic pH. Particular attention is paid to Escherichia coli extreme acid resistance mechanisms, the activity of which ensure survival and may be directly linked to virulence.

]]>
As part of their life cycle, neutralophilic bacteria are often exposed to varying environmental stresses, among which fluctuations in pH are the most frequent. In particular, acid environments can be encountered in many situations from fermented food to the gastric compartment of the animal host. Herein, we review the current knowledge of the molecular mechanisms adopted by a range of Gram-positive and Gram-negative bacteria, mostly those affecting human health, for coping with acid stress. Because organic and inorganic acids have deleterious effects on the activity of the biological macromolecules to the point of significantly reducing growth and even threatening their viability, it is not unexpected that neutralophilic bacteria have evolved a number of different protective mechanisms, which provide them with an advantage in otherwise life-threatening conditions. The overall logic of these is to protect the cell from the deleterious effects of a harmful level of protons. Among the most favoured mechanisms are the pumping out of protons, production of ammonia and proton-consuming decarboxylation reactions, as well as modifications of the lipid content in the membrane. Several examples are provided to describe mechanisms adopted to sense the external acidic pH. Particular attention is paid to Escherichia coli extreme acid resistance mechanisms, the activity of which ensure survival and may be directly linked to virulence.
Neutralophilic bacteria, especially those affecting human health, possess mechanisms that enhance growth in moderate acid (pH 4–6) and enable survival in extreme acid (pH 1–3).
SOS, the formidable strategy of bacteria against aggressionshttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12077SOS, the formidable strategy of bacteria against aggressionsZeynep Baharoglu, Didier Mazel2014-06-30T10:12:47.011489-05:00doi:10.1111/1574-6976.12077John Wiley & Sons, Inc.10.1111/1574-6976.12077http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12077Review Article11261145Abstract

The presence of an abnormal amount of single-stranded DNA in the bacterial cell constitutes a genotoxic alarm signal that induces the SOS response, a broad regulatory network found in most bacterial species to address DNA damage. The aim of this review was to point out that beyond being a repair process, SOS induction leads to a very strong but transient response to genotoxic stress, during which bacteria can rearrange and mutate their genome, induce several phenotypic changes through differential regulation of genes, and sometimes acquire characteristics that potentiate bacterial survival and adaptation to changing environments. We review here the causes and consequences of SOS induction, but also how this response can be modulated under various circumstances and how it is connected to the network of other important stress responses. In the first section, we review articles describing the induction of the SOS response at the molecular level. The second section discusses consequences of this induction in terms of DNA repair, changes in the genome and gene expression, and sharing of genomic information, with their effects on the bacteria's life and evolution. The third section is about the fine tuning of this response to fit with the bacteria's ‘needs’. Finally, we discuss recent findings linking the SOS response to other stress responses. Under these perspectives, SOS can be perceived as a powerful bacterial strategy against aggressions.

Beyond being a repair process, SOS induction leads to a very strong but transient response to genotoxic stress, which potentiates bacterial survival and adaptation to changing environments.

]]>
The presence of an abnormal amount of single-stranded DNA in the bacterial cell constitutes a genotoxic alarm signal that induces the SOS response, a broad regulatory network found in most bacterial species to address DNA damage. The aim of this review was to point out that beyond being a repair process, SOS induction leads to a very strong but transient response to genotoxic stress, during which bacteria can rearrange and mutate their genome, induce several phenotypic changes through differential regulation of genes, and sometimes acquire characteristics that potentiate bacterial survival and adaptation to changing environments. We review here the causes and consequences of SOS induction, but also how this response can be modulated under various circumstances and how it is connected to the network of other important stress responses. In the first section, we review articles describing the induction of the SOS response at the molecular level. The second section discusses consequences of this induction in terms of DNA repair, changes in the genome and gene expression, and sharing of genomic information, with their effects on the bacteria's life and evolution. The third section is about the fine tuning of this response to fit with the bacteria's ‘needs’. Finally, we discuss recent findings linking the SOS response to other stress responses. Under these perspectives, SOS can be perceived as a powerful bacterial strategy against aggressions.
Beyond being a repair process, SOS induction leads to a very strong but transient response to genotoxic stress, which potentiates bacterial survival and adaptation to changing environments.
Bacteria under stress by complement and coagulationhttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12080Bacteria under stress by complement and coagulationEvelien T.M. Berends, Annemarie Kuipers, Marietta M. Ravesloot, Rolf T. Urbanus, Suzan H.M. Rooijakkers2014-09-03T08:45:40.380872-05:00doi:10.1111/1574-6976.12080John Wiley & Sons, Inc.10.1111/1574-6976.12080http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12080Review Article11461171Abstract

The complement and coagulation systems are two related protein cascades in plasma that serve important roles in host defense and hemostasis, respectively. Complement activation on bacteria supports cellular immune responses and leads to direct killing of bacteria via assembly of the Membrane Attack Complex (MAC). Recent studies have indicated that the coagulation system also contributes to mammalian innate defense since coagulation factors can entrap bacteria inside clots and generate small antibacterial peptides. In this review, we will provide detailed insights into the molecular interplay between these protein cascades and bacteria. We take a closer look at how these pathways are activated on bacterial surfaces and discuss the mechanisms by which they directly cause stress to bacterial cells. The poorly understood mechanism for bacterial killing by the MAC will be reevaluated in light of recent structural insights. Finally, we highlight the strategies used by pathogenic bacteria to modulate these protein networks. Overall, these insights will contribute to a better understanding of the host defense roles of complement and coagulation against bacteria.

We take a closer look at how complement and coagulation induce stress to bacterial cells.

]]>
The complement and coagulation systems are two related protein cascades in plasma that serve important roles in host defense and hemostasis, respectively. Complement activation on bacteria supports cellular immune responses and leads to direct killing of bacteria via assembly of the Membrane Attack Complex (MAC). Recent studies have indicated that the coagulation system also contributes to mammalian innate defense since coagulation factors can entrap bacteria inside clots and generate small antibacterial peptides. In this review, we will provide detailed insights into the molecular interplay between these protein cascades and bacteria. We take a closer look at how these pathways are activated on bacterial surfaces and discuss the mechanisms by which they directly cause stress to bacterial cells. The poorly understood mechanism for bacterial killing by the MAC will be reevaluated in light of recent structural insights. Finally, we highlight the strategies used by pathogenic bacteria to modulate these protein networks. Overall, these insights will contribute to a better understanding of the host defense roles of complement and coagulation against bacteria.
We take a closer look at how complement and coagulation induce stress to bacterial cells.
The bacterial translation stress responsehttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12083The bacterial translation stress responseAgata L. Starosta, Jürgen Lassak, Kirsten Jung, Daniel N. Wilson2014-09-26T06:04:16.369703-05:00doi:10.1111/1574-6976.12083John Wiley & Sons, Inc.10.1111/1574-6976.12083http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12083Review Article11721201Abstract

Throughout their life, bacteria need to sense and respond to environmental stress. Thus, such stress responses can require dramatic cellular reprogramming, both at the transcriptional as well as the translational level. This review focuses on the protein factors that interact with the bacterial translational apparatus to respond to and cope with different types of environmental stress. For example, the stringent factor RelA interacts with the ribosome to generate ppGpp under nutrient deprivation, whereas a variety of factors have been identified that bind to the ribosome under unfavorable growth conditions to shut-down (RelE, pY, RMF, HPF and EttA) or re-program (MazF, EF4 and BipA) translation. Additional factors have been identified that rescue ribosomes stalled due to stress-induced mRNA truncation (tmRNA, ArfA, ArfB), translation of unfavorable protein sequences (EF-P), heat shock-induced subunit dissociation (Hsp15), or antibiotic inhibition (TetM, FusB). Understanding the mechanism of how the bacterial cell responds to stress will not only provide fundamental insight into translation regulation, but will also be an important step to identifying new targets for the development of novel antimicrobial agents.

Regulation of protein synthesis under conditions of environmental stress is mediated by a host of ribosome binding factors.

]]>
Throughout their life, bacteria need to sense and respond to environmental stress. Thus, such stress responses can require dramatic cellular reprogramming, both at the transcriptional as well as the translational level. This review focuses on the protein factors that interact with the bacterial translational apparatus to respond to and cope with different types of environmental stress. For example, the stringent factor RelA interacts with the ribosome to generate ppGpp under nutrient deprivation, whereas a variety of factors have been identified that bind to the ribosome under unfavorable growth conditions to shut-down (RelE, pY, RMF, HPF and EttA) or re-program (MazF, EF4 and BipA) translation. Additional factors have been identified that rescue ribosomes stalled due to stress-induced mRNA truncation (tmRNA, ArfA, ArfB), translation of unfavorable protein sequences (EF-P), heat shock-induced subunit dissociation (Hsp15), or antibiotic inhibition (TetM, FusB). Understanding the mechanism of how the bacterial cell responds to stress will not only provide fundamental insight into translation regulation, but will also be an important step to identifying new targets for the development of novel antimicrobial agents.
Regulation of protein synthesis under conditions of environmental stress is mediated by a host of ribosome binding factors.
Nutritional iron turned inside out: intestinal stress from a gut microbial perspectivehttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12086Nutritional iron turned inside out: intestinal stress from a gut microbial perspectiveGuus A.M. Kortman, Manuela Raffatellu, Dorine W. Swinkels, Harold Tjalsma2014-09-29T05:24:12.449638-05:00doi:10.1111/1574-6976.12086John Wiley & Sons, Inc.10.1111/1574-6976.12086http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12086Review Article12021234Abstract

Iron is abundantly present on earth, essential for most microorganisms and crucial for human health. Human iron deficiency that is nevertheless highly prevalent in developing regions of the world can be effectively treated by oral iron administration. Accumulating evidence indicates that excess of unabsorbed iron that enters the colonic lumen causes unwanted side effects at the intestinal host–microbiota interface. The chemical properties of iron, the luminal environment and host iron withdrawal mechanisms, especially during inflammation, can turn the intestine in a rather stressful milieu. Certain pathogenic enteric bacteria can, however, deal with this stress at the expense of other members of the gut microbiota, while their virulence also seems to be stimulated in an iron-rich intestinal environment. This review covers the multifaceted aspects of nutritional iron stress with respect to growth, composition, metabolism and pathogenicity of the gut microbiota in relation to human health. We aim to present an unpreceded view on the dynamic effects and impact of oral iron administration on intestinal host–microbiota interactions to provide leads for future research and other applications.

Oral iron administration, host iron status and intestinal inflammation can have a large impact on the gut microbiota composition, metabolism and virulence. This review comprehensively highlights the multifaceted aspects of nutritional iron stress within the colon lumen.

]]>
Iron is abundantly present on earth, essential for most microorganisms and crucial for human health. Human iron deficiency that is nevertheless highly prevalent in developing regions of the world can be effectively treated by oral iron administration. Accumulating evidence indicates that excess of unabsorbed iron that enters the colonic lumen causes unwanted side effects at the intestinal host–microbiota interface. The chemical properties of iron, the luminal environment and host iron withdrawal mechanisms, especially during inflammation, can turn the intestine in a rather stressful milieu. Certain pathogenic enteric bacteria can, however, deal with this stress at the expense of other members of the gut microbiota, while their virulence also seems to be stimulated in an iron-rich intestinal environment. This review covers the multifaceted aspects of nutritional iron stress with respect to growth, composition, metabolism and pathogenicity of the gut microbiota in relation to human health. We aim to present an unpreceded view on the dynamic effects and impact of oral iron administration on intestinal host–microbiota interactions to provide leads for future research and other applications.
Oral iron administration, host iron status and intestinal inflammation can have a large impact on the gut microbiota composition, metabolism and virulence. This review comprehensively highlights the multifaceted aspects of nutritional iron stress within the colon lumen.
Metal limitation and toxicity at the interface between host and pathogenhttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12087Metal limitation and toxicity at the interface between host and pathogenKyle W. Becker, Eric P. Skaar2014-09-29T05:24:26.078916-05:00doi:10.1111/1574-6976.12087John Wiley & Sons, Inc.10.1111/1574-6976.12087http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12087Review Article12351249Abstract

Metals are required cofactors for numerous fundamental processes that are essential to both pathogen and host. They are coordinated in enzymes responsible for DNA replication and transcription, relief from oxidative stress, and cellular respiration. However, excess transition metals can be toxic due to their ability to cause spontaneous, redox cycling and disrupt normal metabolic processes. Vertebrates have evolved intricate mechanisms to limit the availability of some crucial metals while concurrently flooding sites of infection with antimicrobial concentrations of other metals. To compete for limited metal within the host while simultaneously preventing metal toxicity, pathogens have developed a series of metal regulatory, acquisition, and efflux systems. This review will cover the mechanisms by which pathogenic bacteria recognize and respond to host-induced metal scarcity and toxicity.

]]>
Metals are required cofactors for numerous fundamental processes that are essential to both pathogen and host. They are coordinated in enzymes responsible for DNA replication and transcription, relief from oxidative stress, and cellular respiration. However, excess transition metals can be toxic due to their ability to cause spontaneous, redox cycling and disrupt normal metabolic processes. Vertebrates have evolved intricate mechanisms to limit the availability of some crucial metals while concurrently flooding sites of infection with antimicrobial concentrations of other metals. To compete for limited metal within the host while simultaneously preventing metal toxicity, pathogens have developed a series of metal regulatory, acquisition, and efflux systems. This review will cover the mechanisms by which pathogenic bacteria recognize and respond to host-induced metal scarcity and toxicity.
The cellular requirement for metal homeostasis necessitates that successful pathogens elaborate and regulate metal acquisition and detoxification systems in response to host-imposed nutritional immunity.
Physical stress and bacterial colonizationhttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12088Physical stress and bacterial colonizationMichael Otto2014-09-29T05:24:44.092859-05:00doi:10.1111/1574-6976.12088John Wiley & Sons, Inc.10.1111/1574-6976.12088http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F1574-6976.12088Review Article12501270Abstract

Bacterial surface colonizers are subject to a variety of physical stresses. During the colonization of human epithelia such as on the skin or the intestinal mucosa, bacteria mainly have to withstand the mechanical stress of being removed by fluid flow, scraping, or epithelial turnover. To that end, they express a series of molecules to establish firm attachment to the epithelial surface, such as fibrillar protrusions (pili) and surface-anchored proteins that bind to human matrix proteins. In addition, some bacteria – in particular gut and urinary tract pathogens – use internalization by epithelial cells and other methods such as directed inhibition of epithelial turnover to ascertain continued association with the epithelial layer. Furthermore, many bacteria produce multilayered agglomerations called biofilms with a sticky extracellular matrix, providing additional protection from removal. This review will give an overview over the mechanisms human bacterial colonizers have to withstand physical stresses with a focus on bacterial adhesion.

Bacterial colonizers of human epithelia have a series of means to withstand mechanical removal and other physical stresses, which include in particular surface-attached binding proteins that interact with human matrix components.

]]>
Bacterial surface colonizers are subject to a variety of physical stresses. During the colonization of human epithelia such as on the skin or the intestinal mucosa, bacteria mainly have to withstand the mechanical stress of being removed by fluid flow, scraping, or epithelial turnover. To that end, they express a series of molecules to establish firm attachment to the epithelial surface, such as fibrillar protrusions (pili) and surface-anchored proteins that bind to human matrix proteins. In addition, some bacteria – in particular gut and urinary tract pathogens – use internalization by epithelial cells and other methods such as directed inhibition of epithelial turnover to ascertain continued association with the epithelial layer. Furthermore, many bacteria produce multilayered agglomerations called biofilms with a sticky extracellular matrix, providing additional protection from removal. This review will give an overview over the mechanisms human bacterial colonizers have to withstand physical stresses with a focus on bacterial adhesion.
Bacterial colonizers of human epithelia have a series of means to withstand mechanical removal and other physical stresses, which include in particular surface-attached binding proteins that interact with human matrix components.